Centenary of WWI Armistice, Commemoration, and Memory

As a multidisciplinary team investigating the power of media, the power of representation, and the power of history in connection with the Centenary of WWI armistice, the researchers worked on corpora collected in similar manners as explained above (Sect. 1.4) but from their respective disciplinary perspective, and thus followed different methodologies

Media Discourse of Commemoration. The Centenary of World War One in Europe

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Roundtable: A Multifaceted WWI Centenary and an Evasive Europe

Chapter 9, “Roundtable: A Multifaceted WWI Centenary and an Evasive Europe”, concludes this book. It presents the online roundtable during which the authors shared their results as they pertained to four questions: European belonging, cultural memory and expression of national identity, transnationalization of memory about WWI, and the construction of Europe in news media. This final collective chapter emphasizes the coexisting conceptions of Europe that are present in the media discourse of commemoration. Furthermore, it underlines how the tension between the various national and European narratives regarding the Centenary of WWI is part of an ongoing Europeanization process

Author Correction: Modeling Snyder-Robinson Syndrome in multipotent stromal cells reveals impaired mitochondrial function as a potential cause for deficient osteogenesis.

An amendment to this paper has been published and can be accessed via a link at the top of the paper

Modeling Snyder-Robinson Syndrome in multipotent stromal cells reveals impaired mitochondrial function as a potential cause for deficient osteogenesis.

Patients with Snyder-Robinson Syndrome (SRS) exhibit deficient Spermidine Synthase (SMS) gene expression, which causes neurodevelopmental defects and osteoporosis, often leading to extremely fragile bones. To determine the underlying mechanism for impaired bone formation, we modelled the disease by silencing SMS in human bone marrow - derived multipotent stromal cells (MSCs) derived from healthy donors. We found that silencing SMS in MSCs led to reduced cell proliferation and deficient bone formation in vitro, as evidenced by reduced mineralization and decreased bone sialoprotein expression. Furthermore, transplantation of MSCs in osteoconductive scaffolds into immune deficient mice shows that silencing SMS also reduces ectopic bone formation in vivo. Tag-Seq Gene Expression Profiling shows that deficient SMS expression causes strong transcriptome changes, especially in genes related to cell proliferation and metabolic functions. Similarly, metabolome analysis by mass spectrometry, shows that silencing SMS strongly impacts glucose metabolism. This was consistent with observations using electron microscopy, where SMS deficient MSCs show high levels of mitochondrial fusion. In line with these findings, SMS deficiency causes a reduction in glucose consumption and increase in lactate secretion. Our data also suggests that SMS deficiency affects iron metabolism in the cells, which we hypothesize is linked to deficient mitochondrial function. Altogether, our studies suggest that SMS deficiency causes strong transcriptomic and metabolic changes in MSCs, which are likely associated with the observed impaired osteogenesis both in vitro and in vivo